The aim of ECT is to induce a therapeutic clonic seizure (a seizure where the person loses consciousness and has convulsions) lasting for at least 15 seconds. Although a large amount of research has been carried out, the exact mechanism of action of ECT remains elusive. The main reasons for this are that the human brain can not be studied directly before and after ECT and therefore scientists rely on animal models of depression and ECT, with major limitations. While animal models are acknowledged to model merely aspects of depressive illness, human and animal brains are very similar at a molecular level, enabling detailed study of the molecular mechanisms involved in ECT.

There is a vast literature on the effects of Electroconvulsive Shock (ECS) in animals. In animal models of depression, particularly "Learned helplessness" and "Social defeat", there is evidence of pruning of normally dense synaptic connections in the hippocampus, a richly connected area deep in the temporal lobe which is vital in controlling both mood and memory. ECS has been shown to increase levels of Brain-derived neurotrophic factor (BDNF) and Vascular Endothelial Growth Factor (VEGF) in the rodent hippocampus. This reverses the toxic effects of depression on this area of the brain, increasing both new synapse formation and the formation of new brain cells (hippocampalneurogenesis).

Both these effects have been noted to be present in antidepressant-treated animals, however they are neither necessary nor sufficient for antidepressant response. ECT is a more robust inducer of these neuroplastic effects than antidepressants. Electroconvulsive Therapy (ECT) has also been shown to increase serum brain-derived neurotrophic factor (BDNF) in drug resistant depressed patients. This suggests a common molecular mechanism of action, albeit in need of much further study.